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[Effects of dexamethasone on apoptosis and expression of Fas/FasL system in lung tissues of ALI rats].

AbstractOBJECTIVE:
To determine whether apoptosis occurs in the lung tissues from rats with acute lung injury (ALI), and observe protective effects of dexamethasone by regulating apoptosis of lung tissues in rats with ALI.
METHODS:
By using TUNEL, in situ hybridization, SqRT-PCR and immunocytochemistry techniques, apoptosis and Fas, FasL expression were studied during early phase of ALI in rats.
RESULTS:
LPS leads to the rapid appearance of apoptosis in alveolar epithelial cells and pulmonary vascular endothelial cells at early stage of ALI in rats. The expression of Fas, FasL mRNA and protein was up-regulated in lung tissues of rats with ALI. The administration of dexamethasone suppressed apoptosis as well as expression of Fas, FasL mRNA and protein, inhibited TNF-alpha production and abated lung injury.
CONCLUSIONS:
The excessive apoptosis and Fas/FasL system may play a role in the pathogenesis of LPS-induced ALI in rats. The protective effects of dexamethasone include inhibiting inflammatory mediators production, suppressing the activation of Fas/FasL system and apoptosis in lung tissues of ALI rats.
AuthorsY Song, B Mao, G Qian
JournalZhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases (Zhonghua Jie He He Hu Xi Za Zhi) Vol. 23 Issue 1 Pg. 23-6 (Jan 2000) ISSN: 1001-0939 [Print] China
PMID11778176 (Publication Type: Journal Article)
Chemical References
  • Fas Ligand Protein
  • Faslg protein, rat
  • Membrane Glycoproteins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • fas Receptor
  • Dexamethasone
Topics
  • Animals
  • Apoptosis (drug effects)
  • Dexamethasone (pharmacology)
  • Fas Ligand Protein
  • Lung (metabolism, pathology)
  • Male
  • Membrane Glycoproteins (analysis, genetics)
  • RNA, Messenger (analysis)
  • Rats
  • Rats, Wistar
  • Respiratory Distress Syndrome (drug therapy, metabolism, pathology)
  • Tumor Necrosis Factor-alpha (analysis)
  • fas Receptor (analysis, genetics)

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